European Journal of Heart Failure
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Circulating microRNAs as candidate markers to distinguish heart failure in breathless patients Aims Since their identification in the circulation, microRNAs have received considerable interest as putative biomarkers of cardiovascular disease. We have investigated the diagnostic utility of microRNAs in differentiating between patients with heart failure (HF) and non‐HF‐related breathlessness, and between HF with reduced (HF‐REF) and preserved (HF‐PEF) EF. Methods and results MicroRNA profiling was performed on plasma from 32 HF and 15 COPD patients, as well as 14 healthy controls. Seventeen microRNAs were selected for validation in 44 HF, 32 COPD, 59 other breathless, and 15 controls. Cases of HF were split evenly between HF‐REF and HF‐PEF. Diagnostic utility was compared with NT‐proBNP and high sensitivity troponin T (hs‐troponin T). MiR‐103 [area under the curve (AUC) = 0.642, P = 0.007], miR‐142‐3p (AUC = 0.668, P = 0.002), miR‐199a‐3p (AUC = 0.668, P = 0.002), miR‐23a (AUC = 0.637, P = 0.010), miR‐27b (AUC = 0.642, P = 0.008), miR‐324‐5p (AUC = 0.621, P = 0.023), and miR‐342‐3p (AUC = 0.644, P = 0.007) were associated with HF diagnosis in regression and receiver operating characteristic (ROC) analyses. Individually, NT‐proBNP (AUC = 0.896, P = 9.68 × 10−14 ) and hs‐troponin T (AUC = 0.750, P = 2.50 × 10−6 ) exhibited greater sensitivity and specificity. However, combining significantly associated microRNAs with NT‐proBNP improved the AUC of NT‐proBNP by 4.6% (P = 0.013). Four microRNAs, miR‐103, miR‐142‐3p, miR‐30b, and miR‐342‐3p, were differentially expressed between HF and controls, COPD, and other breathless patients (P = 0.002–0.030). Eight microRNAs that distinguished between HF‐REF and HF‐PEF in screening (P = 0.017–0.049) were not replicated in the validation. Conclusions Four microRNAs distinguished between HF and exacerbation of COPD, other causes of dyspnoea, and controls. Seven were associated with HF diagnosis in regression and ROC analysis. Although individually NT‐proBNP was far superior in predicting HF, combining microRNA levels with NT‐proBNP may add diagnostic value.
European Journal of Heart Failure - Tập 15 Số 10 - Trang 1138-1147 - 2013
Towards better definition, quantification and treatment of fibrosis in heart failure. A scientific roadmap by the Committee of Translational Research of the Heart Failure Association (HFA) of the European Society of Cardiology Abstract Fibrosis is a pivotal player in heart failure development and progression. Measurements of (markers of) fibrosis in tissue and blood may help to diagnose and risk stratify patients with heart failure, and its treatment may be effective in preventing heart failure and its progression. A lack of pathophysiological insights and uniform definitions has hampered the research in fibrosis and heart failure. The Translational Research Committee of the Heart Failure Association discussed several aspects of fibrosis in their workshop. Early insidious perturbations such as subclinical hypertension or inflammation may trigger first fibrotic events, while more dramatic triggers such as myocardial infarction and myocarditis give rise to full blown scar formation and ongoing fibrosis in diseased hearts. Aging itself is also associated with a cardiac phenotype that includes fibrosis. Fibrosis is an extremely heterogeneous phenomenon, as several stages of the fibrotic process exist, each with different fibrosis subtypes and a different composition of various cells and proteins — resulting in a very complex pathophysiology. As a result, detection of fibrosis, e.g. using current cardiac imaging modalities or plasma biomarkers, will detect only specific subforms of fibrosis, but cannot capture all aspects of the complex fibrotic process. Furthermore, several anti‐fibrotic therapies are under investigation, but such therapies generally target aspecific aspects of the fibrotic process and suffer from a lack of precision. This review discusses the mechanisms and the caveats and proposes a roadmap for future research.
European Journal of Heart Failure - Tập 21 Số 3 - Trang 272-285 - 2019
Circulating cardiac autoantibodies in dilated cardiomyopathy and myocarditis: pathogenetic and clinical significance Abstract Dilated cardiomyopathy (DCM) is a relevant cause of heart failure and a common indication for heart transplantation. It may be idiopathic, familial/genetic, viral, autoimmune or immune‐mediated associated with a viral infection. Myocarditis is an inflammatory disease of the myocardium; it may be idiopathic, infectious or autoimmune and may heal or lead to DCM. Thus, in a patient subset, myocarditis and DCM are thought to represent the acute and chronic stages of an organ‐specific autoimmune disease of the myocardium. In keeping with this hypothesis, autoimmune features in patients with myocarditis/DCM include: familial aggregation; a weak association with HLA‐DR4; abnormal expression of HLA class II on cardiac endothelium on endomyocardial biopsy; and detection of organ‐ and disease‐specific cardiac autoantibodies of the IgG class in the sera of affected patients and symptom‐free relatives. The cardiac autoantibodies detected by immunofluorescence are directed against multiple antigens. Two of these, first identified using immunoblotting and confirmed by ELISA, are the atrial‐specific α‐ and the ventricular and skeletal muscle β‐heavy chain isoform. The α‐myosin isoform fulfils the expected criteria for organ‐specific autoimmunity, in that immunization with cardiac, but not skeletal myosin reproduces, in susceptible mouse strains, the human disease phenotype of myocarditis/DCM; in addition, α‐myosin is entirely cardiac‐specific. Additional antigenic targets of heart‐reactive autoantibodies include unknown sarcolemmal proteins, mitochondrial enzymes, β‐adrenergic and muscarinic receptors. For some of these antibodies, there is in vitro evidence for a functional role. The organ‐specific cardiac autoantibodies detected by immunofluorescence in symptom‐free relatives were associated with echocardiographic features suggestive of early disease. Mid‐term follow‐up suggests that these antibodies are predictive markers of progression to DCM among symptom‐free relatives with or without abnormal echocardiographic findings.
European Journal of Heart Failure - Tập 4 Số 4 - Trang 411-417 - 2002
Myocarditis as a precipitating factor for heart failure: evaluation and 1‐year follow‐up using cardiovascular magnetic resonance and endomyocardial biopsy Aims The aim of this study was to evaluate myocarditis as a precipitating factor for heart failure using cardiovascular magnetic resonance (CMR) and endomyocardial biopsy Methods and results Eighty‐five patients with suspected myocarditis and 20 controls were evaluated. Seventy‐one patients with positive CMR were referred for endomyocardial biopsy and re‐evaluation after 1 year. Cardiovascular magnetic resonance was performed using STIR T2‐weighted (T2W), early T1‐weighted (EGE), and late gadolinium‐enhanced (LGE) images. Immunohistological and polymerase chain reaction (PCR) analysis of myocardial specimens was employed. In patients with myocarditis, T2 and EGE were increased compared with controls (2.6 ± 0.9 vs. 1.57 ± 0.13, P < 0.001 and 7.9 ± 5.5 vs. 3.59 ± 0.08, P < 0.001, respectively). Late gadolinium enhancement was found in all myocarditis patients. Endomyocardial biopsy performed in 50 of 71 patients with positive CMR showed positive immunohistology in 48% and presence of infectious genomes in 80% (mainly Chlamydia, Herpes, and Parvovirus B19). Left ventricular ejection fraction (LVEF) was significantly decreased compared with controls (47.7 ± 19.2 vs. 64 ± 0.2, P < 0.001). After 1 year, CMR showed normalization of T2 and EGE, and decreased LGE. Left ventricular ejection fraction increased in 36.5% of patients, remained stable in 56.5% and decreased in 7% of patients, in whom biopsy showed persistence of the initial infective agents. A negative correlation was identified between EGE, LGE, and LVEF. Patients with positive biopsies had lower LVEFs. Conclusion In a Greek population with myocarditis, Chlamydia with viruses was a common finding. Cardiovascular magnetic resonance and PCR proved useful for the detection of myocarditis; EGE and LGE had the best correlation for the development of heart failure. Persistence of the initially detected infective agents was identified in patients who deteriorated further.
European Journal of Heart Failure - Tập 13 Số 8 - Trang 830-837 - 2011
Role of cardiopulmonary exercise testing in clinical stratification in heart failure. A position paper from the Committee on Exercise Physiology and Training of the Heart Failure Association of the European Society of Cardiology Traditionally, the main indication for cardiopulmonary exercise testing (CPET) in heart failure (HF) was for the selection of candidates to heart transplantation: CPET was mainly performed in middle‐aged male patients with HF and reduced left ventricular ejection fraction. Today, CPET is used in broader patients' populations, including women, elderly, patients with co‐morbidities, those with preserved ejection fraction, or left ventricular assistance device recipients, i.e. individuals with different responses to incremental exercise and markedly different prognosis. Moreover, the diagnostic and prognostic utility of symptom‐limited CPET parameters derived from submaximal tests is more and more considered, since many patients are unable to achieve maximal aerobic power. Repeated tests are also being used for risk stratification and evaluation of intervention, so that these data are now available. Finally, patients, physicians and healthcare decision makers are increasingly considering how treatments might impact morbidity and quality of life rather than focusing more exclusively on hard endpoints (such as mortality) as was often the case in the past. Innovative prognostic flowcharts, with CPET at their core, that help optimize risk stratification and the selection of management options in HF patients, have been developed.
European Journal of Heart Failure - Tập 20 Số 1 - Trang 3-15 - 2018
Independent relationship of left atrial size and mortality in patients with heart failure: an individual patient meta‐analysis of longitudinal data (MeRGE Heart Failure) Aims Left atrial (LA) size is considered a marker of poor prognosis in heart failure (HF) patients. Prior studies have recruited relatively few subjects limiting their power to adequately analyse the interaction between LA size, left ventricular (LV) systolic and diastolic function, and prognosis. Method and results The MeRGE collaboration combines prospective data from 18 studies in HF patients. In this analysis of data from 1157 patients, the primary endpoint was death or hospitalization for worsening HF. In multivariate analysis (Cox proportion hazard model), LA area was associated with prognosis (HR 1.03 per cm2 , 95% CI 1.02, 1.05; P < 0.0001) independently of age, NYHA class, LV ejection fraction, and restrictive filling pattern (RFP). When LA area was used as a categorical variable, the HR associated with larger LA area (above median) was 1.4 (95% CI 1.13, 1.74) and when LA area index was used, the HR was 2.36 (95% CI 1.80, 3.08). When the patients with and without RFP were divided on the basis of either LA area or LA area index, significantly higher event rates were observed in those with larger LA area. Conclusion Left atrial area is a powerful predictor of outcome among HF patients with predominantly impaired systolic function, and is independent of, and provides additional prognostic information beyond LV systolic and diastolic function.
European Journal of Heart Failure - Tập 11 Số 10 - Trang 929-936 - 2009
Patient selection criteria and midterm clinical outcome for MitraClip therapy in patients with severe mitral regurgitation and severe congestive heart failure Aims The implantation of a MitraClip (MC) is a new treatment modality for severe mitral regurgitation (MR) in patients whose condition is inoperable or who are at high conventional operative risk. This study reports the follow‐up data of patients implanted with an MC in our heart centre to find selection criteria for this procedure in patients with severe congestive heart failure. Methods and results This study included 163 implantation procedures in 157 patients between March 2009 and November 2012. The severe MR was caused by functional or organic valve disease. The patients had no surgical treatment option or dramatically increased surgical operative risk due to reduced LVEF or concomitant diseases. Three (2%) implantation procedures were unsuccessful. Eleven (7%) patients died during the first 30 days after MC implantation, and 9 (6%) additional patients died during the first 6 months, both groups mainly due to severe, therapy‐resistant end‐stage heart failure. The 111 patients who were followed up showed significant improvement in NT‐proBNP, LVEF, NYHA class, 6 min walk test, and quality of life. Ten (6%) patients needed conventional heart surgery despite high operative risk due to persistent symptomatic MR after MC implantation. Conclusion The interventional implantation of an MC is a new treatment for severe MR with acceptable periprocedural risk and results in clinical improvement in the majority. Patients with end‐stage heart failure and an NT‐proBNP value >10 000 pg/mL have a high mortality despite MC implantation, and their treatment should be based on a very individualized decision. Based on this experience, a clinical algorithm for patient selection is proposed.
European Journal of Heart Failure - Tập 15 Số 7 - Trang 786-795 - 2013
Intramyocardial inflammation predicts adverse outcome in patients with cardiac AL amyloidosis Aims To evaluate the influence of endomyocardial biopsy (EMB)‐proven intramyocardial inflammation on mortality in patients with cardiac transthyretin amyloid (ATTR) or amyloid light‐chain (AL) amyloidosis. Methods and results We included 54 consecutive patients (mean age 68.83 ± 9.59 years; 45 men) with EMB‐proven cardiac amyloidosis. We followed up patients from first diagnostic biopsy to as long as 36 months (mean 11.5 ± 12 months) and compared their outcome with information on all‐cause mortality with or without proof of inflammation on EMB. Intramyocardial inflammation was assessed by quantitative immunohistology. Patients suffering from amyloidosis revealed a significant poor prognosis with proof of intramyocardial inflammation in contrast to those without inflammation (log‐rank P = 0.019). Re‐grouping of patients indicated AL amyloidosis to have a significant impact on all‐cause mortality (log‐rank P = 0.012). The detailed subgroup analysis showed that patients suffering from AL amyloidosis with intramyocardial inflammation have a significantly worse prognosis compared with AL amyloidosis without inflammation and ATTR with or without inflammation, respectively (log‐rank P = 0.014, contingency Fisher's exact test, P = 0.008). Conclusion Our study reports for the first time a high incidence (48.1%) of intramyocardial inflammation in a series of patients with EMB‐proven cardiac amyloidosis and could show that in patients with AL amyloidosis, intramyocardial inflammation correlated significantly with increased mortality. Our data have a direct clinical impact because one can hypothesize that additional immunomodulating/anti‐inflammatory treatment regimens in patients with biopsy‐proven inflammation of heart muscle tissue could be beneficial for patients suffering from cardiac AL amyloidosis.
European Journal of Heart Failure - Tập 20 Số 4 - Trang 751-757 - 2018
Impact of heart failure on the clinical course and outcomes of patients hospitalized for <scp>COVID</scp>‐19. Results of the <scp>Cardio‐COVID‐Italy</scp> multicentre study Abstract Aims To assess the prognostic value of a history of heart failure (HF) in patients with coronavirus disease 2019 (COVID‐19). Methods and results We enrolled 692 consecutive patients admitted for COVID‐19 in 13 Italian cardiology centres between 1 March and 9 April 2020. Mean age was 67.4 ± 13.2 years, 69.5% of patients were males, 90 (13.0%) had a history of HF, median hospitalization length was 14 days (interquartile range 9–24). In‐hospital death occurred in 37 of 90 patients (41.1%) with HF history vs. 126 of those with no HF history (20.9%). The increased risk of death associated with HF history remained significant after adjustment for clinical variables related to COVID‐19 and HF severity, including comorbidities, oxygen saturation, lymphocyte count and plasma troponin [adjusted hazard ratio (HR) for death: 2.25; 95% confidence interval (CI) 1.26–4.02; P = 0.006 at multivariable Cox regression model including 404 patients]. Patients with a history of HF also had more in‐hospital complications including acute HF (33.3% vs. 5.1%, P < 0.001), acute renal failure (28.1% vs. 12.9%, P < 0.001), multiorgan failure (15.9% vs. 5.8%, P = 0.004) and sepsis (18.4% vs. 8.9%, P = 0.006). Other independent predictors of outcome were age, sex, oxygen saturation and oxygen partial pressure at arterial gas analysis/fraction of inspired oxygen ratio (PaO2 /FiO2 ). In‐hospital treatment with corticosteroids and heparin had beneficial effects (adjusted HR for death: 0.46; 95% CI 0.29–0.74; P = 0.001; n = 404 for corticosteroids, and adjusted HR 0.41; 95% CI 0.25–0.67; P < 0.001; n = 364 for heparin). Conclusions Hospitalized patients with COVID‐19 and a history of HF have an extremely poor outcome with higher mortality and in‐hospital complications. HF history is an independent predictor of increased in‐hospital mortality.
European Journal of Heart Failure - Tập 22 Số 12 - Trang 2238-2247 - 2020
Heart failure in COVID‐19 patients: prevalence, incidence and prognostic implications Aims Data on the impact of COVID‐19 in chronic heart failure (CHF) patients and its potential to trigger acute heart failure (AHF) are lacking. The aim of this work was to study characteristics, cardiovascular outcomes and mortality in patients with confirmed COVID‐19 infection and a prior diagnosis of heart failure (HF). Further aims included the identification of predictors and prognostic implications for AHF decompensation during hospital admission and the determination of a potential correlation between the withdrawal of HF guideline‐directed medical therapy (GDMT) and worse outcomes during hospitalization. Methods and results Data for a total of 3080 consecutive patients with confirmed COVID‐19 infection and follow‐up of at least 30 days were analysed. Patients with a previous history of CHF (n = 152, 4.9%) were more prone to the development of AHF (11.2% vs. 2.1%; P < 0.001) and had higher levels of N‐terminal pro brain natriuretic peptide. In addition, patients with previous CHF had higher mortality rates (48.7% vs. 19.0%; P < 0.001). In contrast, 77 patients (2.5%) were diagnosed with AHF, which in the vast majority of cases (77.9%) developed in patients without a history of HF. Arrhythmias during hospital admission and CHF were the main predictors of AHF. Patients developing AHF had significantly higher mortality (46.8% vs. 19.7%; P < 0.001). Finally, the withdrawal of beta‐blockers, mineralocorticoid receptor antagonists and angiotensin‐converting enzyme inhibitors or angiotensin receptor blockers was associated with a significant increase in in‐hospital mortality. Conclusions Patients with COVID‐19 have a significant incidence of AHF, which is associated with very high mortality rates. Moreover, patients with a history of CHF are prone to developing acute decompensation after a COVID‐19 diagnosis. The withdrawal of GDMT was associated with higher mortality.
European Journal of Heart Failure - Tập 22 Số 12 - Trang 2205-2215 - 2020
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